The microenvironment is important for the proliferation and survival of chronic lymphocytic leukemia (CLL) cells.1,2 Various cell types may contribute to provide signals and release factors that prevent apoptosis of CLL cells.3,4 Molecules that facilitate the interaction between the leukemic cells and the microenvironment may be critical in the pathophysiology of CLL and potentially serve as structures for targeted therapies.
In 2001, gene expression profiling in CLL showed an increased expression of the extracellular matrix (ECM) protein fibromodulin (FMOD).5 FMOD is a member of the small leucine-rich proteoglycan family (SLRP) and is normally expressed in collagen-rich tissues. We demonstrated that FMOD was expressed at the gene and protein level in CLL and mantle cell lymphoma (MCL).6 Cluster regulation of genes has been reported in malignant diseases.7 The proline/arginine-rich end leucine-rich repeat protein (PRELP) has a structure closely related to FMOD and is located about 80 kb 3′-proximal to FMOD on chromosome 1q32.1.8 PRELP has a molecular weight (MW) of 55 kDa and is normally expressed in the extracellular matrix of connective tissues, mainly in cartilage, lung, kidney, skin, and tendon.9,10 The function of PRELP is unclear, but the interactions between PRELP and collagen type I and II as well as heparin and heparan sulphates 11,12 suggest that PRELP may be a molecule anchoring basement membranes to connective tissue.12 